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  • 1
    Electronic Resource
    Electronic Resource
    Changes in Cerebral Acyl-CoA Concentrations Following Ischemia-Reperfusion in Awake Gerbils (1997)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 68 (1997), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Transient global cerebral ischemia affects phospholipid metabolism and features a considerable increase in unesterified fatty acids. Reincorporation of free fatty acids into membrane phospholipids during reperfusion following transient ischemia depends on conversion of fatty acids to acyl-CoAs via acyl-CoA synthetases and incorporation of the acyl group into lysophospholipids. To study the effect of ischemia-reperfusion on brain fatty acid and acyl-CoA pools, the common carotid arteries were tied for 5 min in awake gerbils, after which the ligatures were released for 5 min and the animals were killed by microwave irradiation. Twenty percent of these animals (two of 10) were excluded from the ischemia-reperfusion group when it was demonstrated statistically that brain unesterified arachidonic acid concentration was not elevated beyond the range of the control group. Brain unesterified fatty acid concentration was increased 4.4-fold in the ischemic-reperfused animals, with stearic acid and arachidonic acid increasing the most among the saturated and polyunsaturated fatty acids, respectively. The total acyl-CoA concentration remained unaffected, indicating that reacylation of membrane lysophospholipids is maintained during recovery. However, there was a substantial increase in the stearoyl- and arachidonoyl-CoA and a marked decrease in palmitoyl- and docosahexaenoyl-CoA. These results suggest that unesterified fatty acid reacylation into phospholipids is reprioritized according to the redistribution in concentration of acyl-CoA molecular species, with incorporation of stearic acid and especially arachidonic acid being favored.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1997.68052111.x
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  • 2
    Electronic Resource
    Electronic Resource
    Mutant herpes simplex virus induced regression of tumors growing in immunocompetent rats (1994)
    Springer
    Journal of neuro-oncology 19 (1994), S. 137-147 
    Details
    ISSN: 1573-7373
    Keywords: HSV ; thymidine kinase ; ribonucleotide reductase ; viral vector ; anti-tumor effect
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Herpes simplex virus (HSV) mutants kill dividing tumor cells but spare non-proliferating, healthy brain tissue and may be useful in developing new treatment strategies for malignant brain tumors. Two HSV mutants, a thymidine kinase deficient virus (TK-) and a ribonucleotide reductase mutant (RR-), killed 7/7 human tumor cell lines in tissue culture. The TK-HSV killed Rat RG2 glioma and W256 carcinoma lines but not the rat C6 glioma in culture. TK-HSV replication (12 pfu/cell) was similar to wild-type HSV (10 pfu/cell) in rapidly dividing W256 cells in tissue culture, but was minimal (〈1 pfu/cell) in serum-starved cells, suggesting that the proliferative activity of tumor cells at the site and time of TK-HSV injection may influence efficacyin vivo. Subcutaneous W256 tumors in male Sprague-Dawley rats were injected with TK-HSV or virus free inoculum. A significant effect of TK-HSV therapy on W256 tumor growth was demonstrated compared to controls (p=0.002). Complete regression was observed in 4/9 experimental tumors, with no recurrence over 6 months. Tumor growth in the remaining 5/9 animals was attenuated during the first 3 to 5 days after treatment, but not beyond 5 days compared to 9 matched control animals; no tumor regression was observed in any of the control animals. These results suggest that HSV mutants are potentially useful as novel therapeutic agents in the treatment of tumors in immunocompetent subjects.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01306455
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  • 3
    Electronic Resource
    Electronic Resource
    Apparent glucose utilization in Walker 256 metastatic brain tumors (1985)
    Springer
    Journal of neuro-oncology 3 (1985), S. 153-164 
    Details
    ISSN: 1573-7373
    Keywords: glucose utilization ; Walker 256 tumors ; metastatic brain tumors ; deoxyglucose ; quantitative autoradiography
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Regional rates of apparent glucose utilization (GU) in metastatic Walker 256 (WL-256) brain tumors produced by the intracarotid injection of WL-256 tumor cells in rats were measured using14C-deoxyglucose and quantitative auroradiography. Apparent glucose utilization was uniform within individual small and medium size tumors without necrosis, varied considerably among different tumors within this group, and did not correlate with tumor size or location. High values of GU in medium and large-size tumors correlated with viable-appearing tissue in contrast to necrotic tissue and were always 1.3 to 3 times higher than that of adjacent and contralateral nontumorous brain. The apparent net extraction of glucose (E n * ) in viable tumor regions was estimated to be several fold higher than that in remote brain tissue; analysis of this data for medium and large tumors indicates that the calculated values of GU and E n * overestimate the actual rates of utilization and net extraction of glucose. Local cerebral glucose utilization (LCGU) was higher than normal adjacent to small tumors and lower than normal adjacent to large tumors. The LCGU in many gray-matter structures remote from the intracerebral tumors was reduced and roughly proportional to the metastatic tumor burden. The comparatively high uptake of 2-deoxyglucose by viable tumor cells has diagnostic and localization value and suggests that appropriate glucose analogues could be developed to produce a tumor-selective inhibition of glycolysis and tumoricidal effect.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02228892
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  • 4
    Electronic Resource
    Electronic Resource
    Dexamethasone effects on vascular volume and tissue hematocrit in experimental RG-2 gliomas and adjacent brain (1988)
    Springer
    Journal of neuro-oncology 6 (1988), S. 157-168 
    Details
    ISSN: 1573-7373
    Keywords: brain tumors ; vascular volume ; dexamethasone ; gliomas ; tissue hematocrit ; RISA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have studied the effects of dexamethasone, a corticosteroid commonly used to treat brain tumors, on vascular volume and tissue hematocrit in RG-2 experimental rat gliomas.125I-RISA (radioiodinated serum albumin) was used to measure tissue plasma vascular volume (Vp) and51Cr labeled red cells were used to measure tissue red cell volume (Vrbc). Quantitative autoradiography was used to obtain local measurements of Vp and Vrbc in different brain and tumor regions. From these experimentally measured values, we calculated the tissue vascular volume (Vv), tissue hematocrit (THct) and systemic arterial hematocrit (AHct). The value reported primarily reflect capillary and small vessel volumes since blood drained from larger vessels during tissue processing and large vascular structures were avoided during analysis of the autoradiographic images. A total of 110 tumors were studied in 29 animals. There was a consistent trend for Vp and Vv to be reduced in all tumor regions after dexamethasone treatment, although a significant decrease was seen only in tumor center. Dexamethasone did not affect Vp or Vv in tumor-free brain regions. Dexamethasone appeared to have little effect on Vrbc in any brain or tumor region. THct was consistently, although not significantly, higher in tumors after treatment with dexamethasone; THct in tumor-free brain regions was unaffected by dexamethasone treatment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02327392
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  • 5
    Electronic Resource
    Electronic Resource
    Apparent glucose utilization in Walker 256 metastatic brain tumors (1986)
    Springer
    Journal of neuro-oncology 4 (1986), S. 5-16 
    Details
    ISSN: 1573-7373
    Keywords: glucose utilization ; Walker 256 tumors ; metastatic brain tumors ; deoxyglucose ; quantitative autoradiography
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Regional rates of apparent glucose utilization (GU) in metastatic Walker 256 (WL-256) brain tumors produced by the intracarotid injection of WL-256 tumor cells in rats were measured using14C-deoxyglucose and quantitative aroradiography. Apparent glucose utilization was uniform within individual small and medium size tumors without necrosis, varied considerably among different tumors within this group, and did not correlate with tumor size or location. High values of GU in medium and large-size tumors correlated with viable-appearing tissue in contrast to necrotic tissue and were always 1.3 to 3 times higher than that of adjacent and contralateral nontumorous brain. The apparent net extraction of glucose (E n * ) in viable tumor regions was estimated to be several fold higher than that in remote brain tissue; analysis of this data for medium and large tumors indicates that the calculated values of GU and E n * overestimate the actual rates of utilization and net extraction of glucose. Local cerebral glucose utilization (LCGU) was higher than normal adjacent to small tumors and lower than normal adjacent to large tumors. The LCGU in many gray-matter structures remote from the intracerebral tumors was reduced and roughtly proportional to the metastatic tumor burden. The comparatively high uptake of 2-deoxyglucose by viable tumor cells has diagnostic and localization value and suggests that appropriate glucose analogues could be developed to produce a tumor-selective inhibition of glycolysis and tumoricidal effect.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02157996
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